Janet Cross

Cross, Janet V.

Primary Appointment

Associate Professor, Pathology


  • BS, Recombinant Gene Technology, Medical Technology, State University of New York College at Fredonia
  • PhD, Molecular Biology and Microbiology, Case Western Reserve University

Contact Information

Telephone: 434-243-9401
Email: jvc5b@Virginia.EDU

Research Disciplines

Cancer Biology, Experimental Pathology, Immunology, Molecular Biology, Translational Science

Research Interests

Contribution of the Inflammatory Microenvironment to Tumor Initiation, Progression and Metastasis; Molecular Mechanisms of Cancer Chemoprevention

Research Description

The central objective of my lab is to understand how the host immune response is reprogrammed by tumors to promote growth and metastasis. Specifically, we focus on the role of an inflammatory cytokine, the Macrophage Migration Inhibitory Factor (MIF) in cancer. We identified MIF as a target for inhibition by a class of cancer preventive agents present in fresh vegetables, including broccoli. MIF is overexpressed in many cancers, and the degree of overexpression correlates with tumor aggressiveness and metastatic potential. This observation supported our efforts to determine how MIF might contribute to cancer. In recently published work, we have established that MIF promotes tumor growth and is required for tumor metastasis. We demonstrated that MIF carries out its pro-tumor effects through influence over the host immune system, rather than by altering an intrinsic property of the tumor cells. Specifically we discovered that MIF regulates the abundance of a class of immunosuppressive cells within the tumor microenvironment. These cells, monocytic Myeloid Derived Suppressor Cells (Mo-MDSCs) suppress T cell mediated immune responses, thereby protecting the tumor from immune destruction. In this study, we demonstrated that treating tumor bearing mice with our MIF inhibitory compound reduces the abundance of Mo-MDSCs in the tumors, suggesting that we may be able to target MIF therapeutically to inhibit tumor progression through manipulation of the host immune response. The primary goal of ongoing work in our lab is to further understand the mechanisms by which MIF regulates the tumor microenvironment to promote tumor progression. Additionally, we continue to evaluate the potential utility of our inhibitor as a therapeutic approach in other MIF-dependent inflammatory disease processes.

Selected Publications